The shingles resource page

Herpes zoster, colloquially known as shingles, is the reactivation of varicella zoster virus, leading to a crop of painful blisters over the area of a dermatome. In Italy and in Malta, it is sometimes referred to as St. Anthony's fire. Prior to implementation of the universal varicella vaccination program in the U.S., incidence of shingles increased with advancing age. The incidence rate in children aged less than 10 years was approximately 70 cases/100,000 person-years, increasing to 550 cases/100,000 person-years among adults aged 50 to 59 years. Historically, it was thought that shingles incidence increased due to an age-related decline in immunity; however, recent studies ^[1] suggest that incidence of shingles is linked to the reduced frequency of periodic exogenous (outside) exposures to children with varicella (chickenpox) due to the increasing vaccination of that population. These exposures produced an immunologic boost that helped suppress the reactivation of shingles. Shingles incidence is high in the elderly (over 60), as well as in any age group of immunocompromised patients. It affects some 1 million people per year in the United States and can involve excruciating pain. Treatment is generally with antiviral drugs such as aciclovir. Many patients develop a painful condition called postherpetic neuralgia which is often difficult to manage.

In some patients, herpes zoster can reactivate subclinically with pain in a dermatomal distribution without rash. This condition is known as zoster sine herpete and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis.

The word herpes comes from the Greek word for snake; it is cognate with herpetology^[2].

Signs and symptoms

Often, pain is the first symptom. This pain can be characterized as stinging, tingling, numbing, or throbbing, and can be pronounced with quick stabs of intensity. Then 1-3 crops of red lesions develop, which gradually turn into small blisters filled with serous fluid. A general feeling of unwellness often occurs. In some cases, the rash does not form blisters, but has an appearance much like urticaria ("hives").

As long as the blisters have not dried out, HZ patients may transmit the virus to others. This could lead to chickenpox in people (mainly young children) who are not yet immune to this virus.

Chickenpox virus can remain dormant for decades, and does so inside the ganglion near the spinal cord. As the virus is reactivated it spreads down peripheral nerve fibers and produces intense pain. The blisters therefore only affect one area of the body and do not cross the midline. They are most common on the torso, but can also appear on the face (where they are potentially hazardous to vision) or other parts of the body.

Diagnosis

The diagnosis is visual — very few other diseases mimic herpes zoster, especially in the localization of the rash, which is otherwise quite similar in appearance and initial effect to that of poison oak or poison ivy. In case of doubt, fluid from a blister may be analyzed in a medical laboratory.

Pathophysiology

The causative agent for herpes zoster is varicella zoster virus (VZV). Most people are infected with this virus as a child, as it causes chickenpox. The body eliminates the virus from the system, but it remains dormant in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.

Generally, the immune system suppresses reactivation of the virus. In the elderly, whose immune response generally tends to deteriorate, as well as in those patients whose immune system is being suppressed, this process fails. (Some researchers speculate that sunburn and other, unrelated stresses that can affect the immune system may also lead to viral reactivation.) The virus starts replicating in the nerve cells, and newly formed viruses are carried down the axons to the area of skin served by that ganglion (a dermatome). Here, the virus causes local inflammation in the skin, with the formation of blisters.

The pain characteristic of herpes zoster is thought to be due to irritation of the sensory nerve fibers in which the virus reproduces.

Therapy

Aciclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valacyclovir and famciclovir. Steroids are often given in severe cases. During the acute phase oral aciclovir should be given five times daily for 7 to 10 days. Immunocompromised patients may respond best to intravenous aciclovir. In patients who are at high risk for recurrences, an oral dose of aciclovir, taken twice daily, is usually effective. Use of acylovir is most effective in moderating the progress of the symptoms if taken as early as possible, so medical care should be obtained as soon as the condition is recognized.

The long term complication postherpetic neuralgia may cause persistent pain that lasts for years. Pain management is difficult as conventional analgesics may be ineffective. Alternative agents are often used, including tricyclic antidepressants (particularly amitriptyline), anticonvulsants (e.g. gabapentin), and/or topical capscaicin.

Zostavax is a vaccine developed by Merck & Co. which has proven successful in preventing half the cases of herpes zoster in a study of 38,000 people who received the vaccine.^[3] The vaccine also reduced by two-thirds the number of cases of postherpetic neuralgia.^[4] However, prior to the vaccine, it has long been known that adults received natural immune boosting from contact with children infected with varicella. This helped to suppress the reactivation of herpes zoster.^[5] In Massachusetts, herpes zoster incidence increased 90%, from 2.77/1000 to 5.25/1000 in the period of increasing varicella vaccination 1999-2003.^[6] The effectiveness of the varicella vaccine itself is dependent on this exogenous (outside) boosting mechanism. Thus, as natural cases of varicella decline, so has the effectiveness of the vaccine.^[7]

Often the same treatment given to burn victims relieves the pain of shingles, including over-the-counter moist burn pads.

Prognosis

The rash and pain usually subside within 3 to 5 days. The most common chronic complication of herpes zoster is postherpetic neuralgia. Pain that persists for longer than one to three months after resolution of the rash is generally accepted as the sign of postherpetic neuralgia. Sometimes serious effects including partial facial paralysis (usually temporary), ear damage, or encephalitis may occur. Shingles on the upper half of the face (the first branch of the trigeminal nerve) may result in eye damage and require urgent ophthalmological assessment. Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve. These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.

Since shingles is a reactivation of a virus contracted previously—often decades earlier—it cannot be induced by exposure to another person with shingles or chickenpox. Those with active blisters, however, can spread chickenpox to others who have never had that condition and who have not been vaccinated against it.

Stages

References

^ M.N. Oxman et al. The Shingles Prevention Study Group (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine 253 (22): 2271-2284. PMID 15930418.
^ Treatment of Herpes Zoster with Fire Needle retrieved May 22, 2006
^ Oxman MN, Levin MJ, Johnson GR, et al (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". N Engl J Med 352 pages=2271–84. PMID 15930418.
^ M.N. Oxman et al. The Shingles Prevention Study Group (2005). "A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults". New England Journal of Medicine 253 (22): 2271-2284. PMID 15930418.
^ Brisson M, Gay N, Edmunds W, Andrews N (2002). "Exposure to varicella boosts immunity to herpes-zoster: implications for mass vaccination against chickenpox.". Vaccine 20 (19-20): 2500-7. PMID 12057605.
^ W.K. Yih et al. Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care (2005). "The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccination coverage, 1998-2003". BMC Public Health 5 (1): 68-68. PMID 15960856.
^ G.S. Goldman. Medical Veritas Internation Inc. (2005). "Universal varicella vaccination: efficacy trends and effect on herpes zoster". International Journal of Toxicology 24 (4): 205-213. PMID 16126614.

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